The hepatitis C virus chronically infects about 170 million people worldwide. Effective antiviral drug treatments are available. However, because of reinfections, high pharmaceutical costs, and new infections, additional interventions may be needed to bring the global HCV epidemic under control. As a result, there is continued interest in HCV molecular virology, virus-host interactions, and vaccine development.
In 2009, it was discovered that HCV expresses a family of previously-unknown proteins from the core gene (Eng et al., J. Virol., 2009; 83:3104-14; herein incorporated by reference). These minicore proteins have the C-terminal portion of the mature p21 nucleocapsid (core) protein, but lack the N-terminus (see FIG. 1). The estimated sizes of two prominent minicore proteins, 70 and 91 minicore, suggest that they begin at core amino acids 70 and 91, respectively (see FIGS. 1 and 2). Mutations in positions 70 and 91 are associated with an increased risk of hepatocellular carcinoma, insulin resistance, and failure on interferon-based treatments (see Akuta et al., Hepatology, 2007, 46:1357-64; Akuta et al., J. Med. Virol., 2009, 81:1032-9; and Akut a et al., J. Hepatol. 2007, 46:403-10; all of which are herein incorporated by reference), suggesting that minicores may affect clinical outcomes. It was recently found that minicores are secreted into the media in cell culture systems (El-Shamy et al., Hepatology, 2014; 60:1056A; #1782).